There has been an intensive effort in the past year to identify immunologic and nonimmunologic factors in the pathogenesis of cardiac allograft vasculopathy. Significant progress has been made regarding cell proliferation and cell death, with particular focus on cell growth factors, cell death factors, and their receptors. Endothelial cell injury and endothelin expression and production have been implicated in the development of cardiac allograft vasculopathy. A significant clinical association between dyslipidemia and cardiac allograft vasculopathy has been detected by intracoronary ultrasonography. Furthermore, proteoglycans are postulated to play an important role through lipoprotein-proteoglycan interactions. The role of cytomegalovirus infection remains controversial. Immunosuppressive agents such as rapamycin and FK506 may contribute to a reduction of vasculopathy.